DESCRIPTION: Severe trauma, wounds and sepsis result in generalized suppression of host defenses. Mammalian macrophages possess a recently described cell surface receptor that recognizes beta-1,3 polymers of glucose. This beta-glucan receptor provides a means for opsonin- independent recognition and clearance of microorganisms. Binding to beta-glucan receptors potentiates the phagocytic function of macrophages. Receptors for binding the Fc portion of immunoglobulin and the complement receptor are well characterized markers of macrophage activation. These opsonic receptors are known to be compromised in neutrophils from septic animals. The role of the beta-glucan receptor is presently unknown and is the focus of this application. These studies will detail the structure and binding characteristics of the receptor using standard methods to quantitate number and affinity. The expression of beta- glucan will be determined in resting and activated cells from various anatomic sites. Experiments will compare the beta- glucan receptor expression with the expression of opsonic receptors and correlate similarities and differences with activation state and immune function. These studies will test the hypothesis that the non-opsonic beta-glucan receptor plays a greater role in host defense under conditions of compromised opsonin-dependent phagocytosis.